Introduction
Obesity is an unbalanced condition in which accumulated dietary calories exceed the body’s energy consumption. Currently, obesity is one of the most serious health problems all over the world, including in Korea. It is an ongoing problem for the whole of society, as well as for individuals. Obesity is associated with illnesses such as cardiovascular diseases, diabetes, musculoskeletal disorders such as osteoarthritis, and some cancers, and significantly devalues the quality of life
[1]. From a societal perspective, the annual expenditure on controlling diseases related to obesity is astronomical
[2].
Recently, obesity has been hypothetically regarded as a social epidemic in the sense that it can spread from one person to another
[3,4]. There is consistent evidence that obesity is a health concern that spreads by social peer pressure or social contact
[5]. Mathematical modeling of the progression of most infectious diseases is useful to discover the likely outcome of an epidemic or to help in their management. Indeed, mathematical studies indicate that obesity is transmitted socially
[5–8].
In this paper, we applied a new difference equation model to study obesity in Korean adults aged 19–59 years and also projected the findings into the future. The main purpose of this study was to predict the future prevalence of obesity in 19–59-year-old Koreans and to propose some strategies to reduce obesity in Korea. Moreover, we identified important predictive factors of obesity in the Korean adult population.
Materials and Methods
2.1 Model description
We introduce a two-compartmental deterministic mathematical model, a system of difference equations, to predict the evolution of obesity in the Korean population and to propose strategies to reduce its incidence. Basically, the idea of modeling the obesity epidemic comes from the disease model Susceptible-Infected-Susceptible (SIS)
[9].
As in
[8], we divided the 19–59-year-old population in Korea into two subpopulations based on their body mass index {BMI; weight/height
2 (kg/m
2)}. The classes or subpopulations were individuals defined as normal weight
St (BMI, <25) and obese individuals
Ot (BMI, ≥25) according to the definition of WHO
[10].
We regarded obesity as an infectious disease caused by social peer pressure or social contact that influences the probability of transmission of sedentary lifestyle and unhealthy nutritional habits. From this position, let us propose an epidemiological-type model to study the epidemic evolution of obesity. We adopted the following assumptions
[8]:
(1) Once an adult starts an unhealthy lifestyle, he/she would continue it and develop obesity Ot because of this lifestyle. In class Ot, individuals who are able to stop his/her unhealthy lifestyle can move to class St.
(2) Populations of humans are homogeneously mixed, which means the rate of interaction between two different subpopulations is proportional to the product of the numbers in each of the subsets concerned [11,12]. The transit is modeled using the term βStOt
[13].
(3) The subpopulation’s sizes and behaviors with time will decide the dynamic evolution of adulthood obesity.
The model can be described as shown in
Figure 1.
Without loss of generality and for the sake of clarity, the 19–59-year-old adult population is normalized to unity; for all time
t,
St +
Ot = 1. Under the above assumptions, we have the following nonlinear system of difference equations:
The state variables of the model are shown in
Table 1 and parameters used in the model in
Table 2.
Model
(2.1) is analyzed qualitatively to investigate the existence and stability of equilibria. First, we identify the equilibrium of nonlinear system of difference equations
(2.1). We denoted by
(S¯,O¯) the equilibrium points of system
(2.1). Computing the steady state, we obtain two equilibrium points; the disease-free equilibrium (DFE) for
(2.1) is:
and the endemic equilibrium (EE) for
(2.1) is:
DFE (1,0) is locally asymptotically stable if 0 <
ρ +
μ −
β < 2 and the endemic equilibrium
(S¯,O¯)
(2.3) is locally asymptotically stable if
0<ρ+μ−β(S¯−O¯)<2. On the one hand, model
(2.1) can be simplified to the following one difference equation using the assumption
St +
Ot = 1.
O¯=−(ρ+μ−β)+(ρ+μ−β)2+4βμO0/(2β) is a locally asymptotically stable equilibrium of
(2.4) if 0 < (
ρ +
μ −
β)
2 + 4
βμO0 < 4.
Additionally, DFE (1,0) is locally asymptotically stable of
(2.1) if and only if
O¯ is a locally asymptotically stable equilibrium of
(2.4) and the endemic equilibrium
(S¯,O¯)
(2.3) is locally asymptotically stable of
(2.1) if and only if
O¯ is a locally asymptotically stable equilibrium of
(2.4). See
Appendix for details.
2.2 Numerical computation
Parameter estimation was performed to produce the model of the current Korean situation.
First, we need to know the parameters
μ,
S0, and
O0 of the model.
μ is inversely proportional to the mean time spent by an adult in the system. The total 40 years from age 19 to 59 is 2080 weeks (accepting 1 year = 52 weeks) so
μ should be 1/2080.
S0 and
O0 are the proportions of the normal weight and obese populations, respectively, in the 18 years age group. According to the statistical data of the Korea Institute of Sport Science in 2007
[14], the obesity rate of 18-year-old Koreans was 16.4%.
Parameters
β = 0.0009038 and
ρ = 0.0000336 were estimated by least-square method using obesity data (from 1998 to 2008) of the fourth Korea National Health and Nutrition 2008 (
Figure 2)
[15].
Recall
Ot+1 = −
β(
Ot)
2 + (1 +
β −
ρ −
μ)
Ot +
μO0
(2.4). To know the trend of the obese population of 19–59-year-old Koreans, using the parameter in
Table 3, we simulate our model
(2.4) (
Figure 3).
From
Figure 3, we see that the trend of obese population of persons aged 19 to 59 years in Korea increases.
Now, we compare prevention strategy versus treatment by present simulations of the mathematical model and varying some of the parameters. The aim of varying the parameters is to observe how the final prediction can be affected by these changes. This perturbation allows us to propose obesity prevention strategies.
Figures 4 and 5 suppose an increase of physical activity in the obese class
Ot. Consequently, we tried to increase gradually the parameter
ρ from 0% to 2000% initially given
ρ = 0.0000336. In this case, this treatment strategy on obese individuals produces a small improvement.
Figures 6 and 7 suppose a decrease in the social transmission parameter
β. In this case, we tried to reduce gradually the parameter
β from 0% to 100% initially given
β = 0.0009.38. The prevention strategy on the normal-weight individuals produced a bigger improvement than that produced by the previously mentioned treatment strategies.
By simplifying the condition
ρ+μ−β(S¯−O¯), one may see that the DFE
(S¯,O¯) in
(A5) and the endemic equilibrium
(S¯,O¯) in
(A6) are locally asymptotically stable if and only if
O¯ in
(A7) is a locally asymptotically stable equilibrium.